ArticleNeurotoxicity research2013
Role of PGE₂ EP1 receptor in intracerebral hemorrhage-induced brain injury.
Article in Neurotoxicity research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 28 citations in OpenAlex.
- Prostaglandins: Key players in immunomodulation of the nervous system.Neural regeneration research · 2026Article
- Advancing Post-Stroke Depression Research: Insights from Murine Models and Behavioral Analyses.Life (Basel, Switzerland) · 2024Review
- Behavioral Assessment of Sensory, Motor, Emotion, and Cognition in Rodent Models of Intracerebral Hemorrhage.Frontiers in neurology · 2021Review
- Carbon monoxide attenuates vasospasm and improves neurobehavioral function after subarachnoid hemorrhage.Archives of biochemistry and biophysics · 2019Review
- Article
- Pretreatment with Korean red ginseng or dimethyl fumarate attenuates reactive gliosis and confers sustained neuroprotection against cerebral hypoxic-ischemic damage by an Nrf2-dependent mechanism.Free radical biology & medicine · 2019Article
- Genetic Deletion of PGFFrontiers in neuroscience · 2018Article
- Korean Red Ginseng Pretreatment Protects Against Long-Term Sensorimotor Deficits After Ischemic Stroke Likely Through Nrf2.Frontiers in cellular neuroscience · 2018Article
- Efficacy of Laropiprant in Minimizing Brain Injury Following Experimental Intracerebral Hemorrhage.Scientific reports · 2017Article
- Modulators of microglial activation and polarization after intracerebral haemorrhage.Nature reviews. Neurology · 2017Review
- PGE2-EP3 signaling pathway contributes to protective effects of misoprostol on cerebral injury in APP/PS1 mice.Oncotarget · 2016Article
- Deletion of the hemopexin or heme oxygenase-2 gene aggravates brain injury following stroma-free hemoglobin-induced intracerebral hemorrhage.Journal of neuroinflammation · 2016Article
- Intracerebral hemorrhage outcomes following selective blockade or stimulation of the PGE2 EP1 receptor.BMC neuroscience · 2015Article
- Toxic role of prostaglandin E2 receptor EP1 after intracerebral hemorrhage in mice.Brain, behavior, and immunity · 2015Article
- Genetic deletion of the prostaglandin E2 E prostanoid receptor subtype 3 improves anatomical and functional outcomes after intracerebral hemorrhage.The European journal of neuroscience · 2015Article
- Neuroprotective role of prostaglandin PGE2 EP2 receptor in hemin-mediated toxicity.Neurotoxicology · 2015Article
- Article
- Prostaglandin F2α FP receptor antagonist improves outcomes after experimental traumatic brain injury.Journal of neuroinflammation · 2013Article
- Contribution of PGE2 EP1 receptor in hemin-induced neurotoxicity.Frontiers in molecular neuroscience · 2013Article
- Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Prostaglandin E₂ (PGE₂) has been described to exert beneficial and detrimental effects in various neurologic disorders. These conflicting roles of PGE₂ could be attributed to its diverse receptor subtypes, EP1-EP4. At present, the precise role of EP1 in intracerebral hemorrhage (ICH) is unknown. Therefore, to elucidate its possible role in ICH, intrastriatal injection of collagenase was given in randomized groups of adult male wildtype (WT) and EP1 receptor knockout (EP1⁻/⁻)C57BL/6 mice. Functional outcomes including neurologic deficits, rotarod performance, open field activity, and adhesive removal performance were evaluated at 24, 48, and 72 h post-ICH. Lesion volume, cell survival and death, were assessed using Cresyl Violet, and Fluoro-Jade staining, respectively. Microglial activation and phagocytosis were estimated using Iba1 immunoreactivity and fluorescently-labeled microspheres. Following 72 h post-ICH, EP1⁻/⁻ mice showed deteriorated outcomes compared to the WT control mice. These outcomes were demonstrated by elevated neurological deficits, exacerbated lesion volume, and significantly worsened sensorimotor functions. Fluoro-Jade staining showed significantly increased numbers of degenerating neurons and reduced neuronal survival in EP1⁻/⁻ compared to WT mice. To assess in vivo phagocytosis, the number of microspheres phagocytosed by Iba1-positive cells was 145.4 ± 15.4 % greater in WT compared to EP1⁻/⁻ mice. These data demonstrate that EP1 deletion exacerbates neuro-behavioral impairments following ICH, potentially by slowing down/impairing microglial phagocytosis. A better understanding of this EP1 mechanism could lead to improved intervention strategies for hemorrhagic stroke.
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